Atrioventricular block

Atrioventricular block (AV block) is characterized by an interrupted or delayed conduction between the atria and the ventricles. AV blocks are divided into three different degrees depending on the extent of the delay or interruption. First-degree blocks are identifiable on ECG by a prolonged PR interval. Most patients with first-degree block are asymptomatic, and the condition is usually an incidental finding. Second-degree AV blocks are further divided into two different subtypes. Mobitz type I, or Wenckebach, blocks exhibit a progressive prolongation of the PR interval that culminates in a non-conducted P wave (“dropped beat”). Most patients with Mobitz type I blocks are asymptomatic. The Mobitz type II block generates dropped QRS complexes at regular intervals (e.g. 2:1, 3:1, or 3:2), often leading to bradycardia. Symptoms of patients with Mobitz type II block range from fatigue to dyspnea, chest pain, and/or syncope. This fixed second-degree block frequently progresses to a third-degree block. A third-degree AV block involves total interruption of the electrical impulse between the atria and ventricles. The complete absence of conduction results in a ventricular escape mechanism, which may be dangerously slow and result in life-threatening bradycardia or Stokes-Adams attacks. Therefore, a third-degree AV block is an absolute indication for pacemaker placement.

• Physiological: ↑ vagal tone
• Pathophysiological
  • Idiopathic fibrosis of the conduction system
  • Ischemic heart disease
  • Cardiomyopathy (e.g., due to amyloidosis; or sarcoidosis)
  • Infections (e.g., Lyme disease, bacterial endocarditis)
  • Hyperkalemia (> 6.3 mEq/L)
• Iatrogenic
  • Side effect of certain drugs (e.g.,beta blockers, calcium channel blockers, digitalis)
  • Cardiac interventions (e.g., surgery, alcohol septal ablation)

References:^[1][2]

Definition

• PR interval > 200 ms
• No interruption in atrial to ventricular conduction
• Rate of SA node = heart rate

Characteristics

• May be found in healthy individuals, e.g., in athletes with ↑ vagal tone
• Usually asymptomatic
• Often discovered incidentally on ECG

Treatment

• Clinical assessment for underlying diseases (e.g., structural heart diseases, electrolyte imbalances)
• Usually no specific treatment necessary
• Follow-ups to evaluate progression of the disease
• Pacemaker
  • If the patient also exhibits wide QRS complexes on ECG → identify the level of AV block (within or below the bundle of His) using intracardiac electrogram → if conduction time from the bundle of His to the ventricles is > 100 ms: pacemaker placement
  • Patients with neuromuscular disease (e.g., Kearns-Sayre syndrome, myotonic muscular dystrophy)
  • Symptomatic patients: unpleasant awareness of the heartbeat due to loss of atrioventricular synchrony (pacemaker syndrome)

References:^[3][4][5]

Mobitz type I/Wenckebach

Definition

• Progressive lengthening of the PR interval until a beat is dropped; regular atrial impulse does not reach the ventricles (a normal P wave is not followed by a QRS-complex)
• Rate of SA node > heart rate; mostly regular rhythm separated by short pauses, which may lead to bradycardia

Symptoms/clinical findings

• Usually asymptomatic
• May present with symptoms of reduced cardiac output, resulting in hypoperfusion (e.g., dizziness, syncope; ) and bradycardia
• Irregular pulse

Treatment

• Asymptomatic patients
  • Clinical assessment for underlying diseases (e.g., structural heart diseases, electrolyte imbalances)
  • Usually no specific treatment necessary
  • Follow-ups (ECG and cardiac monitoring; ) to evaluate progression of the disease
• Symptomatic patients
  • Hemodynamically stable
    • Monitoring with transcutaneous pacing pads
    • If symptoms not reversible → placement of a permanent pacemaker
  • Hemodynamically unstable
    • Atropine
    • Temporary cardiac pacing (if not responsive to atropine)

Mobitz type II

Definition

• Single or intermittent non-conducted P waves without QRS complexes
• The PR interval remains constant.
• The conduction of atrial impulses to the ventricles follows regular patterns:
  • 2:1 block: regular AV block that inhibits conduction of every other atrial depolarization (P wave) to the ventricles (heart rate = ½ SA node rate)
  • 3:1 block: regular AV block with 3 atrial depolarizations but only 1 atrial impulse that reach the ventricles (heart rate = ⅓ SA node rate)
  • 3:2 block: regular AV block with 3 atrial depolarizations but only 2 atrial impulses that reach the ventricles (heart rate = ⅔ SA node rate)

Symptoms/clinical findings

• Bradycardia → ↓ cardiac output
  • Fatigue
  • Dyspnea
  • Chest pain
  • Dizziness, syncope

Treatment

• Hemodynamically stable patients:
  • Monitoring with transcutaneous pacing pads
  • Clinical assessment for underlying diseases (e.g., structural heart diseases, electrolyte imbalances)
  • If symptoms are not reversible → placement of a permanent pacemaker
• Hemodynamically unstable patients:
  • Atropine
  • Temporary cardiac pacing

The second-degree AV block Mobitz type II may progress to a third-degree block and is an unstable condition that requires monitoring and treatment!

References:^[1][4][6][7]

Definition

• Third-degree AV block is a complete block with no conduction between the atria and ventricles.
• AV dissociation: on ECG, P waves and QRS complexes have their own regular rhythm but bear no relationship to each other
• A ventricular escape mechanism is generated by sites that are usually located near the AV node or near the bundle of His.
  • The more distant the site of impulse generation:
    • The slower the ventricular escape mechanism
    • The wider and more deformed the QRS complex
      • Block proximal to bundle of His: narrow QRS complexes
      • Block distal to bundle of His: wide QRS complexes
    • The worse the prognosis
• Sudden onset of a third-degree AV block results in asystole, which lasts until the ventricular escape mechanism takes over. This asystole may lead to Stokes-Adams attacks.

Symptoms/clinical findings

Symptoms depend on:

• Rate of ventricular escape mechanism
  • Bradycardia (< 40 bpm) with cerebral hypoperfusion (fatigue, irritability, apathy, dizziness, syncope, cognitive impairment), heart failure, dyspnea
• Length of asystole
  • Nausea, dizziness
  • Stokes-Adams attacks
  • Cardiac arrest

Treatment

• Hemodynamically stable patients:
  • Monitoring with transcutaneous pacing pads
  • Clinical assessment for underlying diseases (e.g., structural heart diseases, electrolyte imbalances)
  • No reversible causes → placement of a permanent pacemaker
• Hemodynamically unstable patients:
  • Atropine
  • Temporary transcutaneous or transvenous cardiac pacing
    • In the event of low blood pressure, administer dopamine.
    • In the event of heart failure, administer dobutamine.

References:^[8][9]